Evidence map›Paper›PMID 36227694›Full record

ArticleThe Journal of clinical investigation2022

Meningeal dendritic cells drive neuropathic pain through elevation of the kynurenine metabolic pathway in mice.

Alexandre G Maganin, Guilherme R Souza, Miriam D Fonseca, Alexandre H Lopes, Rafaela M Guimarães, André Dagostin, Nerry T Cecilio, Atlante S Mendes, William A Gonçalves, Conceição Ea Silva and 21 more

Open access · goldAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.2field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  13. Gut microbiota-mediated pain sensitization: mechanisms and therapeutic implications.Frontiers in pain research (Lausanne, Switzerland) · 2025
    Review
  14. Article
  15. Article
  16. Regulatory T cell-derived enkephalin gates nociception.bioRxiv : the preprint server for biology · 2024
    Article
  17. Review
  18. Pathology of pain and its implications for therapeutic interventions.Signal transduction and targeted therapy · 2024
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

31 authors at 4 institutions in 2 countries.

Alexandre G MaganinCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Guilherme R SouzaCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Miriam D FonsecaCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Alexandre H LopesCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Rafaela M GuimarãesCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
André DagostinCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Nerry T CecilioCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Atlante S MendesCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
William A GonçalvesCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Conceição Ea SilvaCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Francisco Isaac Fernandes GomesCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Lucas M Mauriz MarquesCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Rangel L SilvaCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Letícia M ArrudaCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Denis A SantanaCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Henrique LemosCancer Immunology, Inflammation and Tolerance Program, Cancer Center, Georgia Regents University, Augusta, Georgia, USA.
Lei HuangCancer Immunology, Inflammation and Tolerance Program, Cancer Center, Georgia Regents University, Augusta, Georgia, USA.
Marcela Davoli-FerreiraCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Danielle Santana-CoelhoDepartment of Pharmacology, University of Texas Health Science Center at San Antonio and Audie L. Murphy VA Hospital, San Antonio, Texas, USA.
Morena B Sant'AnnaCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Ricardo KusudaCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Jhimmy TalbotCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Gabriela PacholczykCancer Immunology, Inflammation and Tolerance Program, Cancer Center, Georgia Regents University, Augusta, Georgia, USA.
Gabriela A BuquiNPPNS, Department of Physic and Chemistry, School of Pharmaceutical Sciences of Ribeirão Preto, University of Sao Paulo, Ribeirao Preto, Brazil.
Norberto P LopesNPPNS, Department of Physic and Chemistry, School of Pharmaceutical Sciences of Ribeirão Preto, University of Sao Paulo, Ribeirao Preto, Brazil.
Jose C Alves-FilhoCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Ricardo M LeãoDepartment of Physiology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, Brazil.
Jason C O'ConnorDepartment of Pharmacology, University of Texas Health Science Center at San Antonio and Audie L. Murphy VA Hospital, San Antonio, Texas, USA.
Fernando Q CunhaCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Andrew MellorCancer Immunology, Inflammation and Tolerance Program, Cancer Center, Georgia Regents University, Augusta, Georgia, USA.
Thiago M CunhaCenter for Research in Inflammatory Diseases (CRID), Department of Pharmacology and.
Augusta University · USUniversidade de Ribeirão Preto · BRThe University of Texas Health Science Center at San Antonio · USUniversidade de São Paulo · BR

Funding

Cancer Research UK
6 · The paper itself

Abstract

Neuropathic pain is one of the most important clinical consequences of injury to the somatosensory system. Nevertheless, the critical pathophysiological mechanisms involved in neuropathic pain development are poorly understood. In this study, we found that neuropathic pain is abrogated when the kynurenine metabolic pathway (KYNPATH) initiated by the enzyme indoleamine 2,3-dioxygenase 1 (IDO1) is ablated pharmacologically or genetically. Mechanistically, it was found that IDO1-expressing dendritic cells (DCs) accumulated in the dorsal root leptomeninges and led to an increase in kynurenine levels in the spinal cord. In the spinal cord, kynurenine was metabolized by kynurenine-3-monooxygenase-expressing astrocytes into the pronociceptive metabolite 3-hydroxykynurenine. Ultimately, 3-hydroxyanthranilate 3,4-dioxygenase-derived quinolinic acid formed in the final step of the canonical KYNPATH was also involved in neuropathic pain development through the activation of the glutamatergic N-methyl-D-aspartate receptor. In conclusion, these data revealed a role for DCs driving neuropathic pain development through elevation of the KYNPATH. This paradigm offers potential new targets for drug development against this type of chronic pain.

Indexed as

KynurenineNeuralgiaAnimalsDendritic CellsIndoleamine-Pyrrole 2,3,-DioxygenaseMetabolic Networks and PathwaysMiceQuinolinic AcidIndoleamine-Pyrrole 2,3,-DioxygenaseKynurenineQuinolinic AcidAmino acid metabolismDendritic cellsMetabolismNeurosciencePain

Identifiers

PMID36227694
PMCPMC9711882
OpenAlexW4305015463

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.